Loss of bladder control, also known as urinary incontinence, is a widespread, debilitating condition, affecting millions. Associated with symptoms such as sleep deprivation, urosepsis, and skin irritation, urinary incontinence can have significant physiological, psychological, and social impacts on quality of life. The most common form of urinary incontinence, stress urinary incontinence, involves the involuntary leakage of urine upon sneezing, coughing, or other exertion. This leakage generally occurs when an increase in abdominal pressure during a stress event overcomes the body's urinary continence mechanisms.
During urination, muscles in the bladder contract and force urine from the bladder into the urethra. At the same time, the musculature of the urethral wall and the urinary sphincter relax, allowing urine to pass through the urethra and out of the body. During other activity, the urinary sphincter and the musculature of the urethral wall remain contracted, coapting the urethra. The urethra is further supported by a hammock-like pelvic floor which includes endopelvic fascia and, in women, the anterior vaginal wall. Generally, increases in abdominal pressure (generated, for example, by stress events such as coughing or exertion) push the urethra against the pelvic floor, further coapting the urethra.
Stress urinary incontinence is thought to occur by one, or both, of two mechanisms. The first mechanism results from failure of the urinary sphincter and musculature of the urethral wall. In this mechanism, called intrinsic sphincter deficiency, the urethral sphincter muscles are unable to adequately constrict the urethra, which results in urine loss during stress events. Intrinsic sphincter deficiency may result from operative trauma, scarring, denervation or atrophy. The second mechanism, urethral hypermobility, occurs when support structures within the pelvic floor become weakened or damaged. In these cases, the pelvic floor no longer properly functions to compress the urethra upon increases in abdominal pressure.
Fecal incontinence results from a loss of bowel control and an inability to hold stool within the body. During defecation, muscles in the rectum contract and force stool through the anus. Simultaneously, sphincters of the anus relax, thereby allowing stool to pass out of the body. During other activity, the anal sphincters remain contracted, preventing passage of stool therethrough.
Fecal incontinence is thought to be caused by one, or more, of a number of mechanisms. Constipation can result in the stretching and eventual weakening of the rectal muscles, which makes the rectum unable to adequately contain stool. Similarly, physical damage to the internal or external anal sphincters may result in a similar effect. In some situations, nerve damage resulting from childbirth, a stroke or physical injury may prevent the anal sphincters from functioning properly.
Given the widespread and debilitating nature of urinary and fecal incontinence, additional devices for treating urinary and fecal incontinence would be desirable. In particular, adjustable devices, which may allow physicians to change, following or during implantation, the amount of support a device provides would be desirable. Devices that dynamically provide different levels of support during times of stress would also be desirable.